Cardiac Resuscitation Flashcards
Cardiac anatomy
myocardium - cardiac muscle, made of cardiomyocytes
Pericardium - outermost layer of heart
Pericardial sac - Fluid-filled sac surrounding heart
Coronary circulation is mechanism for perfusion of the myocardium.
Endocardium - innermost layer of heart
4 heart chambers: 2 atria and 2 ventricles
Cardiac output
4-8 L/min
average adult is 5.5
Q = HR x SV
Heart valves
tricuspid (right) and mitral valves (left) allow blood into ventricles. Open and close at same time.
pulmonic (left) and aortic valves (right) allow blood out of ventricles. Semilunar valves. Open and close at same time.
Tricuspid valve
3-leaf, low-pressure valve. AV valve
Separates right atrium from right ventricle
Right atrial pressure (central venous pressure): 2-6 mmHg
Right ventricular pressure: 0-5 mmHg
80% of preload is reliant on the function of the AV node, allowing for passive flow.
Remaining 20% of preload is from atrial contraction.
Pulmonic valve (semilunar)
Maintains diastolic pressure
Separates right ventricle from pulmonary artery (only artery to carry deoxygenated blood).
Mitral valve (aka bicuspid)
bicuspid valve (2 cusps). AV Valve.
Separates left atrium from left ventricle
High pressure valve
Aortic valve (semilunar)
most important to maintain cardiac output
Separates left ventricle from aorta/body
preload dependent
heart pressures (L vs R)
left side: high pressure
right side: low pressure
cardiac cycle anatomy
SA node fires, tricuspid valve opens, passive filling of blood from right atrium into right ventricle (diastole).
AV node slows conduction long enough for preload to happen passively.
After right ventricle fills, tricuspid valve closes and first phase of preload is complete. S1 sound.
Next, blood moves out of right ventricle through pulmonic valve to pulmonary artery (to lungs for oxygenation). This squeezing of the ventricles to eject blood out of heart is called isovolumetric contraction. When semilunar valves close, S2 sound.
Blood returns to left atrium from lungs via the pulmonary veins (left atrial preload).
Blood moves to from left atrium to left ventricle (high pressure side) through mitral valve.
Diastole
heart at rest
During diastole, blood fills right atrium from inferior and superior vena cava.
Blood also fills left atrium from pulmonary veins.
Coronary arteries and heart muscle are perfused.
systole
cardiac contraction phase
no cardiac perfusion
SA node rate
Sinoatrial node - primary pacemaker
60-100 bpm
AV node rate
Atrioventricular node - secondary pacemaker
40-60 bpm
AV node delays conduction for RV filling
Heart tones
S1
Mitral and tricuspid closure (AV)
…“lub” sound
S2
Aortic and pulmonic closure (semilunar)
…“dub” sound
S3
passive LV filling, striking compliant LV
Found in athletes with high cardiac output
“Ken-TUCKy” sound
S4 - Active LV filling when atrial contraction forces blood into a noncompliant left ventricle.
…pathalogic. “Ten-nessee”
Cardiac physiology part 2
Cardiac Conduction
SA node
AV node
Bundle of His
Right bundle branch
Left bundle branch
…left posterior fascicle
…left anterior fascicle. Most common for conduction problem
Purkinje fibers: 15-40 bpm
cardiac cycle electrophysiology
P-wave: depolarization of atria in response to SA node firing (atria contracts). Bump up on EKG
PR interval: delay of AV node allowing RV to fill. Flat on EKG while electrical signal passes through AV node.
Q-wave: septal depolarization (depolarization moving through bundle branches). Short sharp bump down on EKG
R-wave: ventricular depolarization
QRS Complex: depolarization of the ventricles which triggers pumping contraction…blood leaves right ventricle into pulmonic valve OR blood leaves left ventricle into aorta to body.
ST segment - beginning of ventricle repolarization
T-wave: ventricular repolarization (re-setting of the heart so it can fire again)
Path of blood through heart/body
Deoxygenated blood enters RIGHT ATRIUM from inferior and superior vena cava
Blood flows from RIGHT ATRIUM through tricuspid valve into right ventricle
RIGHT VENTRICLE pumps deoxygenated blood through pulmonary valve into pulmonary artery and on to the lungs.
Blood is oxygenated in lungs
Oxygenated blood from lungs returns to heart through pulmonary veins into LEFT ATRIUM.
Blood flows from left atrium through mitral valve into LEFT VENTRICLE.
Left ventricle pumps oxygenated blood through aorta to rest of body.
Then deoxygenated blood returns to right atrium and process starts over.
Atrioventricular (AV) valves
Tricuspid and mitral (bicuspid).
Tricuspid separates RA and RV.
Mitral (bicuspid) separates LA and LV.
AV valves are open during diastole and closed during systole to prevent regurgitation.
Semilunar valves
Aortic and pulmonic
Aortic separates LV and aorta
Pulmonary separates RV and pulmonary artery.
Semilunar valves are open during systole and closed during diastole
J-point
start of ST segment.
Normal J-point is at isoelectric line
J-point below line = ischemia
J-point above line = pt progressing in disease process.
right coronary artery
comes off of aorta
blood flow to RCA during diastole when aortic valve is closed.
Supplies blood to right ventricle, right atrium, SA node, and AV node.
Supplies inferior wall, posterior wall.
Most of anterior heart
Occlusion causes changes such as 1st and 2nd degree AV blocks and Mobitz type 1.
Left coronary artery
Circulation during diastole.
Feeds high and low lateral wall.
Left anterior descending - anterior surface of left ventricle.
Supplies blood to left atrium and left ventricle.
New systolic murmur after inferior MI
Most recent cause - mitral regurgitation
Posterior wall MI
Depression or reciprocal changes in nV2-V4 w/associated inferior wall MI (II, III, aVF)
RCA leads on EKG
II, III, aVF
Inferior
Left main / LAD leads on EKG
V1, V2, V3, V4
Anterior
LCx Branch leads on EKG
I, aVL, (High lateral)
V5, V6 (lower lateral)
Left Main insufficiency on EKG
aVR
inferior leads on EKG
II, III, aVF
Anterior leads on EKG
V1, V2, V3, V4
Collateral Circulation
Vessels created to provide an alternate route of circulation to distal areas of the heart.
…Usually presents as a result of aging.
Ramus Intermedius
20-30% of population has this branch.
Lateral wall vessel
Evolution of Occlusion MI (hyper acute)
Early changes suggestive of OMI
Tall and peaked T-waves
…T-waves should be asymmetric.
…symmetrical T waves indicate ischemia
May precede clinical symptoms
Only seen in Leeds looking at infarction areas
Not used as a diagnostic finding.
Evolution of Occlusion MI (Acute)
ST segment elevation (1-2mm elevation)
Implies myocardial injury occurring
Elevated ST segment presumed acute rather than old.
Physiologic Q wave:
<0.04 sec or <1mm wide
<1/3 R wave height or <2mm deep
Pathologic Q wave:
Pathologic = late finding and/or old injury
>0.04 sec or >1mm wide
>1/3 R wave height or >2mm deep
All Q waves in V2-V3
Coronary arteries (2 main)
Right and left coronary arteries
branch from aorta
Left coronary artery
Branches into:
1. Left anterior descending (LAD)
Multiple septal branches off of LAD
Septal branches perfuse intrarventricular septum
Also multiple diagonal branches off of LAD
Diagonal branches perfuse Anteriolateral left ventricle.
- Left circumflex (LCX)
Wraps around circumference of heart.
First branch off of LCX is left atrial artery to perfuse left atrium.
Next branch is obtuse (left) marginal artery
3rd branch (not everybody). Ramus
perfuses anterior lateral wall.
Right Coronary Artery
Comes from right side of aorta
Perfuses right atrium, right atrium, SA and AV nodes
1st branch: Conus artery
2nd: Sinoatrial nodal artery: perfuses SA node
3rd: right atrial branch. Perfuses right atrium
4th: Acute marginal artery. Perfuses right ventricle.
wraps around to back of heart, then…
Atrioventricular nodal artery: perfuses AV node
RCA then bifurcates:
Right posteriolateral artery (RPL): inferiolateral / posteriolateral wall
Posterior Descending Artery (PDA): perfuses inferior / posterior wall - left and right ventricle.
RCA on EKG: II, III, aVF (inferior leads)
Coronary Sinus (vein)
Drains deoxygenated blood back into right atrium
EKG interpretation approach
- Look at V1 to r/in or r/out BBB
- Look for ST elevation segments
…(1, aVL), then (II, III, aVF), then (V1 - V5) - Look for reciprocal changes
…aVL and III are twins, mimic each other
…When both have ST elevation it’s confirmation of a high lateral wall MI
Bundle branch block
QRS > 120 mS or 0.12
Symmetrical T-waves
Indicate ischemia
Inferior wall MI (preload)
Preload problem
Often right ventricular infarction (RVI)
LEOPARD (EKG)
Left ventricular hypertrophy
Early depolarization
Osborn waves
Pericarditis
Aberrant Conduction (LBBB)
Raised ICP
Device (Paced rhythm)
Left Ventricular Hypertrophy (EKG)
LVH recognition = kissing QRS
…Deep QS waves that move deep into lead below.
S wave depth in V1 plus tallest R wave in V5-V6. >35mm diagnostic for LVH
aVL R wave > 11mm = LVH
aVF R wave > 20mm = LVH
Only 1 of these indications needs to be positive to identify LVH.
If positive for LVH, pt probably not a candidate for STEMI activation
Early (benign) repolarization (EKG)
Common in black males 20-40 yrs old
Normal physiology.
Tall waves
Osborn waves (EKG)
(osborn) J wave morphology
first identified in hypothermia (<30C)
Indicative of a slow deflection of uncertain origin.
Also seen in hypercalcemia, secondary to hyperparathyroidism
>3.4 mmol/L or >14 mg/dL
Pericarditis (EKG)
Pericarditis = inflammation of pericardial sac.
Sharp chest pain
radiates to base of neck
pts unable to lay supine
often recent viral illness
ST elevation throughout 12-lead ekg (as opposed to specific area of heart)
PR intervals are down-sloping (tell-tale sign of pericarditis)
Aberrant Conduction (EKG)
BBB criteria = V1 QRS > 0.12 or 120ms
Negatively deflected QRS = LBBB
Positively deflected QRS = RBBB
Old vs new
LBBB will cause ST elevation but pt may not need Cath lab
Raised ICP (EKG)
High sympathetic tone
Increased norepinephrine leads to (deep, >10mm) inverted t-waves
Device (paced) (EKG)
R wave progression
…Negative R wave deflection in V1, but by V6, …(?)
Wide QRS across EKG
Looks like ST elevation
WALDO
Wellen’s syndrome
aVR lead abnormalities
LBBB
De Winter’s T wave
Out of Hospital ROSC
Wellen’s Syndrome (EKG)
…pain free
…normal to slight elevation in cardiac markers
…biphasic t waves in V2-V3 (2 angles)
Deep symmetric t waves in precordial leads
Severe Proximal LAD stenosis
>75% pts will proceed to anterior wall MI within a few weeks.
NO significant ST elevation occurs.
Type 1: uploading ST. Biphasic t-wave V2-3
Type 2: negative and symmetric t-wave
WALDO
aVR (diagnostic) (EKG)
ST elevation in aVR that’s greater than ST elevation in V1, AND anterior depression, that’s highly suggestive of left main insufficiency.
Often progresses to significant MI if not treated.
WALDO
LBBB (EKG)
V1 QRS >0.12 or 120ms
LBBB = negative QRS deflection
RBBB = positive QRS deflection
WALDO
Sgarbossa Criteria
Is LBBB causing MI?
- Concordant ST elevation >1mm
- ST depression >1mm in V1, V2, or V3
- Discordant ST elevation >5mm
…negative deflected QS wave, and positive deflected ST segment
Score greater than 3 is diagnostic for MI
WALDO
De Winter’s T wave (EKG)
Tall prominent T waves
…hyperacute T waves = ischemia
Uploading ST segment depression >1mm
Absence of ST segment elevation in precordial leads
ST segment elevation in aVR
Normal ST morphology
WALDO
Out of hospital ROSC (EKG)
What prompted ROSC??
If pt received sodium bicarb then ROSC, they likely have a pH issue.
WALDO
SHIP
Subtle inferior wall MIs
Hyperacute T waves
Isolated Posterior MIs
Subtle inferior wall MIs (EKG)
0.5mm ST depression in aVL is 97% accurate in identifying inferior wall MI
Reciprocal changes in aVL should lead you to look down at lead III
SHIP
Subtle high lateral wall MIs
Can be identified based on reciprocal changes - lead III
Reciprocal changes in lead III should lead you to look at aVL
SHIP
Hyperacute T waves (EKG)
First indicator of occlusionn
short duration
indication of ischemia
SHIP
Isolated posterior MIs (EKG)
Isolated Posterior wall MI <3.3% of MIs
Often paired w/inferior or lateral MI
Reciprocal changes seen in V1-V4
Mirror image of anterior wall OMI
SHIP
Agonists and antagonists
Agonists - occupy receptors and activate them
Antagonists - occupy receptors but do not activate them. Antagonists block receptor activation by agonists.
Beta blockers
“-lol” drugs
ie metoprolol, labetolol, propranolol
Antagonists of the beta receptors in the heart and lungs.
Slow HR, decrease BP
Esmolol
beta blocker
antagonizes Beta-1 adrenergic receptors
indications: SVT, uncontrolled HTN
Adults: bolus w/500mcg/kg/min over 1 min then start infusion @50mcg/kg/min. Titrate q5min.
Precautions: asthma, bradycardia, AV blocks, CHF.
labetalol
antihypertensive, non-selective beta antagonist.
Adult dosing: 10-20mg slow IVP q10min up to max dose 300mg.
Precautions: asthma, cariogenic shock, 1st degree heart block, severe bradycardia
Calcium channel blockers
Diltiazem, nicardipine (Cardene), nifedipine (Procardia)
Blocks Ca++ influx into smooth muscle - vascular smooth muscle relaxation especially at coronary arteries.
Slows impulses through SA and AV node
Nicardipine (Cardene)
Calcium channel blocker
Indications: HTN
Doses: adults start at 5mg/hr IV, increase by 2.5mg/hr q5-15 min to max 15 mg/hr
Precautions: pregnancy, CHF
Clevidipine
Calcium channel blocker
Antihypertensive, ischemic stroke HTN management
Initial infusion 1-2mg/hr IV, titration of 1-2mghr will produce additional 2-4 mmHg decrease in SBP
Precautions: soy or egg sensitivity
Vasopressors and Inotropes
Dopamine
Epinephrine
Dobutamine
Norepinephrine
Phenylephrine
Vasopressin
Vasopressor causes vasoconstriction
Inotrope increases force of cardiac contraction.
Inopressors
Sympathomimetic (adrenergic) agents
…ie dopamine, norepinephrine
Stimulate Beta 1 receptors, increase contractility, increase HR
Indications: Acute LV failure, low CO states - low perfusion states, Vasogenic shock
Dopamine
Inopressor
Increases contractility
Increases cardiac output
Increases renal perfusion
5-10mcg/kg/min most therapeutic
more is NOT better
Norepinephrine (levophed)
Stimulates alpha adrenergic receptors
Constriction of all vessels and increase in peripheral vascular resistance.
Increases SBP and DBP
Indications: vasogenic shock with tachycardia, sepsis, neurogenic shock.
Dosing: 0.01-2mcg/kg/min or 2-30 mcg/min IV infusion
Inodilators
id dobutamine, milrinone
Sympathomimetic (adrenergic) agents.
Increase contractility
Indications: acute LV failure, pulmonary vasoconstriction, low perfusion states.
Dobutamine
Inodilator
Mild vasodilation
Use caution in borderline hypotensive patients.
Drops systemic vascular resistance
Always fill the tank…
Dosing: 2-20mcg/kg/min
Milrinone
Inodilator
Indications: ischemic and non ischemic cardiomyopathy, CHF
Dosing: 20mg/100ml NS or 40mg/100mL NS
Vasopressors
Vasopressin, Neo-synephrine, methylene blue
Increase BP by constricting vessels
Indications: profound neurogenic shock, push dose pressors, vasogenic shock, refractory septic shock.
phenylephrine
vasopressor
Stimulates alpha receptors
Increases BP without tachycardia
Indications: vasogenic shock esp w/tachycardia, sepsis, neurogenic shock.
Dosing: drip rate typically 10-100mcg/min loading dose followed by maintenance dose 40-60 mcg/min
Vasopressin
vasopressor
Used in pts w/refractory shock despite adequate fluid resuscitation
Indications: vasodilatory shock, septic shock
Dosing: 0.01-0.04 units/min
UGIB: 0.5 units/min
Methylene blue
vasopressor
Indications: vasodilatory shock, septic shock
Dosing 1.5-2 mg/kg over 20 min-1hr
Vasodilators
Action: venous - reduce preload
arterial - reduce afterload.
Indications: HTN, heart failure, cariogenic shock, CAD, PVD
hydralazine
vasodilator
Directly dilates arterial system
decreases afterload
Indications: PIH, HTN
Dosing: 5-10 mg IV
Nitroglycerin
vasodilator
Dilates venous system (decreases preload)
Higher doses dilate arterial system (decreases afterload), improves myocardial O2 consumption
Indications: angina, MI
Adult dosing: 0.5mg SL q5min OR 5mcg/min IV increasing by 5-20 mcg/minn q3-5 min
Nitroprusside
vasodilator
Relaxes vascular smooth muscle
Reduces preload and afterload
Indications: HTN w/complications (hemorrhagic stroke), cariogenic shock, acute aortic dissection
Precautions: pregnancy, cyanide toxicity
Dosing: 0.5-10 mcg/kg/min titrated q5min
Heparinn
Indications: any condition caused by a blood clot (DVT, OMI, ischemic CVA, PE
Precautions: recent major surgery, ulcer, GIB, renal dysfunction
Dosing: Bolus 60-80 units/kg often max of 5k units, then infusion of 15-18 units/kg/hr
ALteplase (activase, t-PA)
Ischemic stroke
STEMI
PE
dosing varies for each use
Axis deviation
Left axis - points away
right axis - points together
Left axis pathologic
-31 to -90 degrees
Rule out:
LVH
Left anterior fascicular block
LBBB
Inferior wall MI
Paced rhythm
right axis deviation
+90 to +180
Chronic (old)
RVH, COPD
Lateral wall MI (pathologic Q waves)
Left posterior hemi block
Acute (new onset)
Misplaced leads
PE
Sodium channel blocker OD
…TCAs, cocaine
Bi-fascicular block (meds)
Left anterior / left posterior block plus RBBB = bi-fascicular block
RBBB is red flag for bi-fascicular block
NEVER administer sodium channel blockers
…No Amiodarone, lidocaine, or procainamide
Cardiovert (only) if necessary…no meds
